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Hyperacute respiratory failure causing transient left ventricular dysfunction
Letters to the Editor
chiatric Association (DSM–IV) (2), do, indeed, feature in the autonomic questionnaire we used. What they have omitted to mention is that our questionnaire contains 20 further questions over and above the nine they refer to, which do not form part of the DSM–IV criteria for panic attacks or other forms of psychiatric disease. None of our patients experienced “a discrete period of intense fear or discomfort in the absence of real danger” that forms “an essential feature” of the criteria for panic attack as defined in DSM–IV (2), and none expressed phobic symptoms. The assertion by Bulbena et al that our patients’ symptoms are psychogenic rather than dysautonomic in origin is highly contentious. Furthermore, it totally ignores the objective laboratory evidence of autonomic dysfunction demonstrated in 78% of the patients in our series presented in our paper. We would agree that the myriad constellation of varying symptoms described in dysautonomias does overlap with some of the criteria defining panic disorders. However, dysautonomia can never be diagnosed solely on symptoms because of their nonspecific nature. The most widely known dysautonomias are defined on the basis of relevant symptoms, plus objective hemodynamic abnormalities, together with (in some cases) coexisting neurological pathology. By contrast, panic disorders are based solely on criteria relating to symptoms. Moreover, there is no evidence of autonomic abnormalities in patients with panic attacks (as extensively studied by Stein et al) (3). None of our patients had evidence of previous psychiatric illnesses (although 1 patient who had taken part in the questionnaire part of the study only had once been prescribed antidepressants). Our criteria for autonomic dysfunction were based on welldefined and widely accepted classification criteria for dysautonomia; e.g., 784
June 1, 2004
postural orthostatic tachycardia syndrome (4). Yael Gazit, MD A. Menahem Nahir, MD, PhD B. Giris Jacob, MD, DSc Israel Institute of Technology, and Rambam Medical Center Haifa, Israel Rodney Grahame, MD University College London Hospitals London, United Kingdom 1. Gazit Y, Nahir AM, Grahame R, Jacob G. Dysautonomia in the hypermobility syndrome. Am J Med. 2003;115:33–40. 2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. (DSM-IV). 4th ed. Arlington, Virginia: American Psychiatric Press; 2000. 3. Stein MB, Asmundson G. Autonomic function in panic disorder: cardiorespiratory and plasma catecholamine responsivity to multiple challenges of the autonomic nervous system. Biol Psychiatry. 1994;36:548 – 558. 4. Schondorf R, Low P. Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia? Neurology. 1993;43:132–137.
HYPERACUTE RESPIRATORY FAILURE CAUSING TRANSIENT LEFT VENTRICULAR DYSFUNCTION To the Editor: A 69-year-old woman with obstructive lung disease presented with moderate respiratory distress; arterial blood gases on 2L O2 were normal except for arterial partial pressure of oxygen (PaO2) of 105 torr. Shortly thereafter, arterial saturation of oxygen (SaO2) fell abruptly to 70%, requiring emergency intubation. Postintubation pH was 6.96, arterial partial pressure of carbon dioxide (PaCO2) was 133 torr, and PaO2 was 114 torr (50% fraction of inspired ox-
THE AMERICAN JOURNAL OF MEDICINE威
Volume 116
ygen [FIO2]). The electrocardiogram demonstrated sinus tachycardia at 127 beats per minute and ST elevation in leads V3 through V6. At 12 hours, echocardiography showed hypokinesis of the apex and midanteroseptal and midlateral walls, with an ejection fraction of 35%. Marked precordial T-wave inversions occurred by 36 hours (Figure). Creatine kinase– MB level peaked at 16 IU and troponin I level peaked at 3.3 ng/mL. On day 2, coronary angiography demonstrated minor irregularities in the left anterior descending and circumflex arteries. Ejection fraction was 50%, with apical hypokinesis. Results of the electrocardiogram were normal 2 weeks later. A 40-year-old woman with asthma and dander allergy presented in extremis hours after bathing her dog. She was unable to speak, was severely cyanotic, and had collapsed. Intubation revealed epiglottal edema. The electrocardiogram showed sinus tachycardia at 104 beats per minute and 0.5 mm of ST elevation in lead I. Postintubation (100% FIO2) pH was 7.02, PaCO2 was 77 torr, and PaO2 was 183 torr. Creatine kinase–MB level peaked at 17 IU and troponin I level at 1.7 ng/mL. One day later, the left ventricular ejection fraction was 25% with global hypokinesis. T-wave inversions appeared in leads I, aVL, and V1 and V2 on day 2 and were normal 3 weeks later. Results of coronary angiography and left ventriculography were normal 4 weeks later. Our patients’ cardiac abnormalities are analogous to those associated with acute subarachnoid hemorrhage (1). Are the mechanisms causing cardiac dysfunction in subarachnoid hemorrhage relevant in our patients? Hyperacute respiratory failure likely initiates a transient, extraordinary sympathetic nervous system discharge. In an animal model of subarachnoid hemorrhage there is an abrupt sympathetic surge (2), cardiac alterations occur almost immediately, and peak values of creatine ki-
Letters to the Editor 7. Janssens U, Koch KC, Graf J, et al. Severe transmyocardial ischemia in a patient with tension pneumothorax. Crit Care Med. 2000;28:1638 –1641. 8. Akashi YJ. Reversible left ventricular dysfunction ’takotsubo’ cardiomyopathy associated with pneumothorax. Heart. 2002;87: E1.
PRIMARY ACTINOMYCOSIS OF THE HUMERUS: A QUITE UNUSUAL FORM Figure. Marked T-wave changes are evident. Serum electrolytes were all normal.
nase-MB and troponin T correlate with peak values of epinephrine and norepinephrine (2). A similar neurohumoral response to subarachnoid hemorrhage occurs in humans (3), and coronary artery disease has been excluded as the cause of the myocardial dysfunction (1). Importantly, in an animal model, pretreatment with propranolol and phentolamine prevents myocardial dysfunction (4). There are similarities in our cases and reports from Japan of a novel syndrome of transient ventricular dysfunction occurring in association with acute emotional or physical stress, including respiratory distress. The syndrome was named “takotsubo” (octopus trap) cardiomyopathy, based on the systolic configuration of the abnormal left ventricle (5). The time course and type of ventricular dysfunction in this syndrome resemble that seen with acute subarachnoid hemorrhage. Three case reports of acute respiratory distress, one with acute asthma and two with severe tension pneumothorax, also have some features similar to our cases (6 – 8). The cardiac abnormalities of our cases parallel those reported with both subarachnoid hemorrhage and the tako-tsubo cardiomyopathy. We postulate that the myocardial injury seen in our patients was a conse-
quence of transient and extraordinary sympathetic activity in the presence of severe hypoxemia. Mehdi Pajouh, MD Robert C. Bahler, MD Case Western Reserve University School of Medicine Heart and Vascular Center MetroHealth Medical Center Cleveland, Ohio
1. Sakr YL, Ghosn I, Vincent JL. Cardiac manifestations after subarachnoid hemorrhage: a systematic review of the literature. Prog Cardiovasc Dis. 2002;45:67–80. 2. Masuda T, Sato K, Yamamoto S, et al. Sympathetic nervous activity and myocardial damage immediately after subarachnoid hemorrhage in a unique animal model. Stroke. 2002;33:1671–1676. 3. Espiner EA, Leikis R, Ferch RD, et al. The neuro-cardio-endocrine response to acute subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2002;56:629 –635. 4. Neil-Dwyer G, Walter P, Cruickshank JM, et al. Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid haemorrhage. BMJ. 1978;2:990 – 992. 5. Kurisu S, Sato H, Kawagoe T, et al. Takkotsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndorme mimicking acute myocardial infarction. Am Heart J. 2002;143:448 –455. 6. Myrianthefs MM, Zambartas CM. Acute, reversible myocardial ischemia in a patient with an asthmatic attack. J Electrocardiol. 1996;29:337–339. June 1, 2004
To the Editor: Primary actinomycosis infection of an extremity is an uncommon feature (1–3). We report a case of a young man with no history of trauma who developed osteomyelitis of the humerus caused by Actinomyces without a known primary infectious focus. A 28-year-old healthy man with a history of relapsing oral infections was admitted to the hospital because he had pain and deformity in his left arm after lifting a 10-kg weight. He had a 3-week history of pain in his left arm without fever or other symptoms and he was taking analgesics. On physical examination, the middle third of his left arm appeared swollen and hot. The rest of the examination was unremarkable. The peripheral white blood cell count showed leukocytosis (16,000 U/L), erythrocyte sedimentation rate was 25 mm/h, and C-reactive protein level was 5.5 mg/dL (reference: 0 to 1 mg/dL). No other laboratory parameters were prominent. A radiograph revealed a fracture line, multiple radiolucent areas, and sclerosis of the periosteum in the distal third of the left humerus (Figure). Gallium (Ga 67) bone scan displayed increased uptake in the same area. The diagnosis of osteomyelitis was made. Results of a bone biopsy showed chronic osteomyelitis, and bacterial colonies of Actinomyces were identified. Gram-positive bacilli susceptible to penicillin, erythromycin, clarithromycin, and
THE AMERICAN JOURNAL OF MEDICINE威
Volume 116 785
chiatric Association (DSM–IV) (2), do, indeed, feature in the autonomic questionnaire we used. What they have omitted to mention is that our questionnaire contains 20 further questions over and above the nine they refer to, which do not form part of the DSM–IV criteria for panic attacks or other forms of psychiatric disease. None of our patients experienced “a discrete period of intense fear or discomfort in the absence of real danger” that forms “an essential feature” of the criteria for panic attack as defined in DSM–IV (2), and none expressed phobic symptoms. The assertion by Bulbena et al that our patients’ symptoms are psychogenic rather than dysautonomic in origin is highly contentious. Furthermore, it totally ignores the objective laboratory evidence of autonomic dysfunction demonstrated in 78% of the patients in our series presented in our paper. We would agree that the myriad constellation of varying symptoms described in dysautonomias does overlap with some of the criteria defining panic disorders. However, dysautonomia can never be diagnosed solely on symptoms because of their nonspecific nature. The most widely known dysautonomias are defined on the basis of relevant symptoms, plus objective hemodynamic abnormalities, together with (in some cases) coexisting neurological pathology. By contrast, panic disorders are based solely on criteria relating to symptoms. Moreover, there is no evidence of autonomic abnormalities in patients with panic attacks (as extensively studied by Stein et al) (3). None of our patients had evidence of previous psychiatric illnesses (although 1 patient who had taken part in the questionnaire part of the study only had once been prescribed antidepressants). Our criteria for autonomic dysfunction were based on welldefined and widely accepted classification criteria for dysautonomia; e.g., 784
June 1, 2004
postural orthostatic tachycardia syndrome (4). Yael Gazit, MD A. Menahem Nahir, MD, PhD B. Giris Jacob, MD, DSc Israel Institute of Technology, and Rambam Medical Center Haifa, Israel Rodney Grahame, MD University College London Hospitals London, United Kingdom 1. Gazit Y, Nahir AM, Grahame R, Jacob G. Dysautonomia in the hypermobility syndrome. Am J Med. 2003;115:33–40. 2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. (DSM-IV). 4th ed. Arlington, Virginia: American Psychiatric Press; 2000. 3. Stein MB, Asmundson G. Autonomic function in panic disorder: cardiorespiratory and plasma catecholamine responsivity to multiple challenges of the autonomic nervous system. Biol Psychiatry. 1994;36:548 – 558. 4. Schondorf R, Low P. Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia? Neurology. 1993;43:132–137.
HYPERACUTE RESPIRATORY FAILURE CAUSING TRANSIENT LEFT VENTRICULAR DYSFUNCTION To the Editor: A 69-year-old woman with obstructive lung disease presented with moderate respiratory distress; arterial blood gases on 2L O2 were normal except for arterial partial pressure of oxygen (PaO2) of 105 torr. Shortly thereafter, arterial saturation of oxygen (SaO2) fell abruptly to 70%, requiring emergency intubation. Postintubation pH was 6.96, arterial partial pressure of carbon dioxide (PaCO2) was 133 torr, and PaO2 was 114 torr (50% fraction of inspired ox-
THE AMERICAN JOURNAL OF MEDICINE威
Volume 116
ygen [FIO2]). The electrocardiogram demonstrated sinus tachycardia at 127 beats per minute and ST elevation in leads V3 through V6. At 12 hours, echocardiography showed hypokinesis of the apex and midanteroseptal and midlateral walls, with an ejection fraction of 35%. Marked precordial T-wave inversions occurred by 36 hours (Figure). Creatine kinase– MB level peaked at 16 IU and troponin I level peaked at 3.3 ng/mL. On day 2, coronary angiography demonstrated minor irregularities in the left anterior descending and circumflex arteries. Ejection fraction was 50%, with apical hypokinesis. Results of the electrocardiogram were normal 2 weeks later. A 40-year-old woman with asthma and dander allergy presented in extremis hours after bathing her dog. She was unable to speak, was severely cyanotic, and had collapsed. Intubation revealed epiglottal edema. The electrocardiogram showed sinus tachycardia at 104 beats per minute and 0.5 mm of ST elevation in lead I. Postintubation (100% FIO2) pH was 7.02, PaCO2 was 77 torr, and PaO2 was 183 torr. Creatine kinase–MB level peaked at 17 IU and troponin I level at 1.7 ng/mL. One day later, the left ventricular ejection fraction was 25% with global hypokinesis. T-wave inversions appeared in leads I, aVL, and V1 and V2 on day 2 and were normal 3 weeks later. Results of coronary angiography and left ventriculography were normal 4 weeks later. Our patients’ cardiac abnormalities are analogous to those associated with acute subarachnoid hemorrhage (1). Are the mechanisms causing cardiac dysfunction in subarachnoid hemorrhage relevant in our patients? Hyperacute respiratory failure likely initiates a transient, extraordinary sympathetic nervous system discharge. In an animal model of subarachnoid hemorrhage there is an abrupt sympathetic surge (2), cardiac alterations occur almost immediately, and peak values of creatine ki-
Letters to the Editor 7. Janssens U, Koch KC, Graf J, et al. Severe transmyocardial ischemia in a patient with tension pneumothorax. Crit Care Med. 2000;28:1638 –1641. 8. Akashi YJ. Reversible left ventricular dysfunction ’takotsubo’ cardiomyopathy associated with pneumothorax. Heart. 2002;87: E1.
PRIMARY ACTINOMYCOSIS OF THE HUMERUS: A QUITE UNUSUAL FORM Figure. Marked T-wave changes are evident. Serum electrolytes were all normal.
nase-MB and troponin T correlate with peak values of epinephrine and norepinephrine (2). A similar neurohumoral response to subarachnoid hemorrhage occurs in humans (3), and coronary artery disease has been excluded as the cause of the myocardial dysfunction (1). Importantly, in an animal model, pretreatment with propranolol and phentolamine prevents myocardial dysfunction (4). There are similarities in our cases and reports from Japan of a novel syndrome of transient ventricular dysfunction occurring in association with acute emotional or physical stress, including respiratory distress. The syndrome was named “takotsubo” (octopus trap) cardiomyopathy, based on the systolic configuration of the abnormal left ventricle (5). The time course and type of ventricular dysfunction in this syndrome resemble that seen with acute subarachnoid hemorrhage. Three case reports of acute respiratory distress, one with acute asthma and two with severe tension pneumothorax, also have some features similar to our cases (6 – 8). The cardiac abnormalities of our cases parallel those reported with both subarachnoid hemorrhage and the tako-tsubo cardiomyopathy. We postulate that the myocardial injury seen in our patients was a conse-
quence of transient and extraordinary sympathetic activity in the presence of severe hypoxemia. Mehdi Pajouh, MD Robert C. Bahler, MD Case Western Reserve University School of Medicine Heart and Vascular Center MetroHealth Medical Center Cleveland, Ohio
1. Sakr YL, Ghosn I, Vincent JL. Cardiac manifestations after subarachnoid hemorrhage: a systematic review of the literature. Prog Cardiovasc Dis. 2002;45:67–80. 2. Masuda T, Sato K, Yamamoto S, et al. Sympathetic nervous activity and myocardial damage immediately after subarachnoid hemorrhage in a unique animal model. Stroke. 2002;33:1671–1676. 3. Espiner EA, Leikis R, Ferch RD, et al. The neuro-cardio-endocrine response to acute subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2002;56:629 –635. 4. Neil-Dwyer G, Walter P, Cruickshank JM, et al. Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid haemorrhage. BMJ. 1978;2:990 – 992. 5. Kurisu S, Sato H, Kawagoe T, et al. Takkotsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndorme mimicking acute myocardial infarction. Am Heart J. 2002;143:448 –455. 6. Myrianthefs MM, Zambartas CM. Acute, reversible myocardial ischemia in a patient with an asthmatic attack. J Electrocardiol. 1996;29:337–339. June 1, 2004
To the Editor: Primary actinomycosis infection of an extremity is an uncommon feature (1–3). We report a case of a young man with no history of trauma who developed osteomyelitis of the humerus caused by Actinomyces without a known primary infectious focus. A 28-year-old healthy man with a history of relapsing oral infections was admitted to the hospital because he had pain and deformity in his left arm after lifting a 10-kg weight. He had a 3-week history of pain in his left arm without fever or other symptoms and he was taking analgesics. On physical examination, the middle third of his left arm appeared swollen and hot. The rest of the examination was unremarkable. The peripheral white blood cell count showed leukocytosis (16,000 U/L), erythrocyte sedimentation rate was 25 mm/h, and C-reactive protein level was 5.5 mg/dL (reference: 0 to 1 mg/dL). No other laboratory parameters were prominent. A radiograph revealed a fracture line, multiple radiolucent areas, and sclerosis of the periosteum in the distal third of the left humerus (Figure). Gallium (Ga 67) bone scan displayed increased uptake in the same area. The diagnosis of osteomyelitis was made. Results of a bone biopsy showed chronic osteomyelitis, and bacterial colonies of Actinomyces were identified. Gram-positive bacilli susceptible to penicillin, erythromycin, clarithromycin, and
THE AMERICAN JOURNAL OF MEDICINE威
Volume 116 785